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TOPK and PTEN participate in CHFR mediated mitotic checkpoint()
Mitotic progression is regulated by co-ordinated action of several proteins and is crucial for the maintenance of genomic stability. CHFR (Check point protein with FHA and RING domains) is an E3 ubiquitin ligase and a checkpoint protein that regulates entry into mitosis. But the molecular players in...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Science Ltd
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819987/ https://www.ncbi.nlm.nih.gov/pubmed/24012691 http://dx.doi.org/10.1016/j.cellsig.2013.08.013 |
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author | Shinde, Swapnil R. Gangula, Narmadha Reddy Kavela, Sridhar Pandey, Vimal Maddika, Subbareddy |
author_facet | Shinde, Swapnil R. Gangula, Narmadha Reddy Kavela, Sridhar Pandey, Vimal Maddika, Subbareddy |
author_sort | Shinde, Swapnil R. |
collection | PubMed |
description | Mitotic progression is regulated by co-ordinated action of several proteins and is crucial for the maintenance of genomic stability. CHFR (Check point protein with FHA and RING domains) is an E3 ubiquitin ligase and a checkpoint protein that regulates entry into mitosis. But the molecular players involved in CHFR mediated mitotic checkpoint are not completely understood. In this study, we identified TOPK/PBK, a serine/threonine kinase and PTEN, a lipid phosphatase to play an important role in CHFR mediated mitotic transitions. We demonstrated that CHFR ubiquitinates and regulates TOPK levels, which is essential for its checkpoint function. Moreover, TOPK phosphorylates and inactivates PTEN, which in turn activates Akt that leads to proper G2/M progression. Collectively, our results reveal TOPK and PTEN as new players in CHFR mediated mitotic checkpoint. |
format | Online Article Text |
id | pubmed-3819987 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Elsevier Science Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-38199872013-12-01 TOPK and PTEN participate in CHFR mediated mitotic checkpoint() Shinde, Swapnil R. Gangula, Narmadha Reddy Kavela, Sridhar Pandey, Vimal Maddika, Subbareddy Cell Signal Article Mitotic progression is regulated by co-ordinated action of several proteins and is crucial for the maintenance of genomic stability. CHFR (Check point protein with FHA and RING domains) is an E3 ubiquitin ligase and a checkpoint protein that regulates entry into mitosis. But the molecular players involved in CHFR mediated mitotic checkpoint are not completely understood. In this study, we identified TOPK/PBK, a serine/threonine kinase and PTEN, a lipid phosphatase to play an important role in CHFR mediated mitotic transitions. We demonstrated that CHFR ubiquitinates and regulates TOPK levels, which is essential for its checkpoint function. Moreover, TOPK phosphorylates and inactivates PTEN, which in turn activates Akt that leads to proper G2/M progression. Collectively, our results reveal TOPK and PTEN as new players in CHFR mediated mitotic checkpoint. Elsevier Science Ltd 2013-12 /pmc/articles/PMC3819987/ /pubmed/24012691 http://dx.doi.org/10.1016/j.cellsig.2013.08.013 Text en © 2013 The Authors https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license |
spellingShingle | Article Shinde, Swapnil R. Gangula, Narmadha Reddy Kavela, Sridhar Pandey, Vimal Maddika, Subbareddy TOPK and PTEN participate in CHFR mediated mitotic checkpoint() |
title | TOPK and PTEN participate in CHFR mediated mitotic checkpoint() |
title_full | TOPK and PTEN participate in CHFR mediated mitotic checkpoint() |
title_fullStr | TOPK and PTEN participate in CHFR mediated mitotic checkpoint() |
title_full_unstemmed | TOPK and PTEN participate in CHFR mediated mitotic checkpoint() |
title_short | TOPK and PTEN participate in CHFR mediated mitotic checkpoint() |
title_sort | topk and pten participate in chfr mediated mitotic checkpoint() |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819987/ https://www.ncbi.nlm.nih.gov/pubmed/24012691 http://dx.doi.org/10.1016/j.cellsig.2013.08.013 |
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